Alterations in body fluid metabolism that result in result in relative deficiencies of water or sodium produce compensatory increases in thirst and sodium appetite, respectively. The general aim of my research is to understand the physiological bases for these drives, and their integration with complementary physiological contributions to homeostasis. In the past few years I have abandoned the traditional view of thirst and sodium appetite as being stimulated by alterations in specific body fluid compartments, and now view the stimuli for these drives from the perspective of the changes they cause in the activity of neuronal systems mediating cerebral arousal. Central catecholamine-containing neurons have been demonstrated to be of critical importance to behavioral activation, and it is stimulation of these neurons during thirst that provides the present model for motivation. The specific aims of the proposed research are to evaluate this model by determining (1) the effect of thirst stimuli on activity in central catecholaminergic neurons, (2) the importance of the pressor and disposogenic effects of the renin-angiotensin system in rats after treatment with various hypotensive agents, (3) the effects of hypovolemia on thirst and sodium appetite in sheep, (4) the effects of hypovolemia on drinking behavior and on the activity of residual dopaminergic neurons in rats with dopamine-depleting brain lesions, and (5) the effects of hypovolemia on the maintenance of blood pressure and on the activity of the sympathoadrenal system in rats after peripheral sympathectomy.